The invention relates to proteins involved in platelet secretion.
Vascular injury can cause a rapid loss of the protein, fluid, and cellular components of the blood. Therefore, animals have developed rapid responses to stop bleeding and to initiate repair of blood vessels. These rapid responses are initiated by the platelet, a highly specialized cell that reacts to vascular injury. Normally, platelets circulate in the blood as quiescent and nonadherent cells, monitoring the integrity of blood vessels. In response to vascular injury, platelets adhere to each other and to de-endothelialized areas, and they undergo activation.
Platelet activation results in morphologic and functional changes in the cell. When platelets are activated by thrombin or other agonists, there is a marked increase in the level of intracellular calcium ions, and an increase in phosphorylation of intracellular proteins. Upon activation, platelet granules fuse with the cell membrane. This leads to platelet secretion of effector molecules, including platelet-derived growth factor, TGF-.beta., clotting factor V, fibrinogen, arachidonate, ADP, and P-selectin. Such molecules secreted by activated platelets play critical roles in the complex cellular and biochemical processes that reduce blood loss and begin the process of vascular repair.
The cellular and biochemical processes initiated by platelets in response to vascular injury can be lifesaving, but in the absence of such injury these same processes can be deleterious. For example, unregulated arterial platelet thrombosis can occlude the blood supply to organs and lead to strokes, heart attacks, and limb necrosis.